Carbohydrate ingestion attenuates cognitive dysfunction following long-duration exercise in the heat in humans.

INTRODUCTION: To determine if electrolyte or carbohydrate supplementation vs. water would limit the magnitude of dehydration and decline in cognitive function in humans following long-duration hyperthermic-exercise. METHODS: 24 subjects performed 3 visits of 2 h walking (3mph/7% grade) in an environmental chamber (33 °C/10% relative humidity). In random order, subjects consumed water (W), electrolytes (Gatorade Zero; E), or electrolytes+carbohydrates (Gatorade; E+C). Throughout exercise (EX), subjects carried a 23 kg pack and drank ad-libitum. Pre-and post-EX, body mass (BM) and plasma osmolality (pOsm) were measured. Physiological Strain Index (PSI) and core temperature (TC) were recorded every 15 min. Plasma glucose (GLU) was measured every 30 min. Cognitive processing (SCWT) was measured post-EX and compared to baseline (BL). A subset of 8 subjects performed a normothermic (N) protocol (21 °C/ambient humidity) to ascertain how the exercise stimulus influenced hydration status and cognition without heat. RESULTS: There were no significant differences between fluid conditions (W, E, E+C) for BM loss (Δ2.5 ± 0.2, 2.5 ± 0.2, 2.3 ± 0.2 kg), fluid consumption (1.9 ± 0.2, 1.9 ± 0.2, 1.8 ± 0.2L), pOsm (Δ1.5 ± 2.7, 2.2 ± 2.4, 2.0 ± 1.5 mmol/L), peak-PSI (7.5 ± 0.4, 7.0 ± 0.6, 7.9 ± 0.5), and peak-TC (38.7 ± 0.1, 38.6 ± 0.2, 38.8 ± 0.2 °C). GLU decreased significantly in W and E, whereas it increased above BL in E+C at 60, 90, and 120 min (P < 0.05). Compared to BL values (43.6 ± 26 ms), SCWT performance significantly decreased in all conditions (463 ± 93, 422 ± 83, 140 ± 52 ms, P < 0.05). Importantly, compared to W and E, the impairment in SCWT was significantly attenuated in E+C (P < 0.05). As expected, when compared to the heat-stress protocol (W, E, E+C), N resulted in lower BM loss, fluid consumption, and peak-PSI (1.1 ± 0.1 kg, 1.2 ± 0.7L, 4.8, respectively), and improved SCWT performance. CONCLUSIONS: These data are the first to suggest that, independent of supplementation variety, cognitive processing significantly decreases immediately following long-duration exercise in the heat in healthy humans. Compared to water and fluids supplemented with only electrolytes, fluids supplemented with carbohydrates significantly blunts this decrease in cognitive function.

Regional influence of nitric oxide on cutaneous vasodilatation and sweating during exercise-heat stress in young men.

NEW FINDINGS: What is the central question of this study? Do regional differences exist in nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and sweating during exercise-heat stress in young men. What is the main finding and its importance? Exercise-induced increases in cutaneous vasodilatation and sweating were greater on the chest and upper back compared to the forearm, although the NOS contribution to cutaneous vasodilatation was similar across all regions. Conversely, there was a greater NOS-dependent rate of change in sweating on the chest compared to the forearm, with a similar trend on the back. ABSTRACT: While it is established that nitric oxide synthase (NOS) is an important modulator of forearm cutaneous vasodilatation and sweating during an exercise-heat stress in young men, it remains unclear if regional differences exist in this response. In 15 habitually active young men (24 ± 4 (SD) years), cutaneous vascular conductance (CVC) and local sweat rate (LSR) were assessed at three body regions. On each of the dorsal forearm, chest and upper-back (trapezius), sites were continuously perfused with either (1) lactated Ringer solution (control) or (2) 10 Mm Nω -nitro-l-arginine (l-NNA, NOS inhibitor), via microdialysis. Participants rested in the heat (35°C) for ∼75 min, followed by 60 min of semi-recumbent cycling performed at a fixed rate of heat production of 200 W m-2 (equivalent to ∼42% V̇O2peak ). During exercise, the chest and upper-back regions showed higher CVC and LSR responses relative to the forearm (all P < 0.05). Within each region, l-NNA attenuated CVC and LSR relative to control (all P < 0.05). However, the NOS contribution was not different across regions for the rate of change and plateau for CVC or for the LSR plateau (all P > 0.05). Conversely, there was a greater NOS contribution to the rate of change for LSR at the chest relative to the forearm (P < 0.05) with a similar trend for the back. In habitually active young men, NOS-dependent cutaneous vasodilatation was similar across regions while the NOS contribution to LSR was greater on the chest relative to the forearm. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilatation and sweating during an exercise-heat stress.

Influence of Sodium Citrate Supplementation after Dehydrating Exercise on Responses of Stress Hormones to Subsequent Endurance Cycling Time-Trial in the Heat.

Background and objectives: In temperate environments, acute orally induced metabolic alkalosis alleviates exercise stress, as reflected in attenuated stress hormone responses to relatively short-duration exercise bouts. However, it is unknown whether the same phenomenon occurs during prolonged exercise in the heat. This study was undertaken with aim to test the hypothesis that ingestion of an alkalizing substance (sodium citrate; CIT) after dehydrating exercise would decrease blood levels of stress hormones during subsequent 40 km cycling time-trial (TT) in the heat. Materials and Methods: Male non-heat-acclimated athletes (n = 20) lost 4% of body mass by exercising in the heat. Then, during a 16 h recovery period prior to TT in a warm environment (32 °C), participants ate the prescribed food and ingested CIT (600 mg·kg-1) or placebo (PLC) in a double-blind, randomized, crossover manner with 7 days between the two trials. Blood aldosterone, cortisol, prolactin and growth hormone concentrations were measured before and after TT. Results: Total work performed during TT was similar in the two trials (p = 0.716). In CIT compared to PLC trial, lower levels of aldosterone occurred before (72%) and after (39%) TT (p ˂ 0.001), and acute response of aldosterone to TT was blunted (29%, p ˂ 0.001). Lower cortisol levels in CIT than in PLC trial occurred before (13%, p = 0.039) and after TT (14%, p = 0.001), but there were no between-trial differences in the acute responses of cortisol, prolactin or growth hormone to TT, or in concentrations of prolactin and growth hormone before or after TT (in all cases p > 0.05). Conclusions: Reduced aldosterone and cortisol levels after TT and blunted acute response of aldosterone to TT indicate that CIT ingestion during recovery after dehydrating exercise may alleviate stress during the next hard endurance cycling bout in the heat.

Impact of sodium citrate ingestion during recovery after strenuous exercise in the heat on heart rate variability: A randomized, crossover study.

Changes in hydration status influence plasma volume (PV) which is associated with post-exercise parasympathetic reactivation. The present study hypothesized that, after dehydrating cycling exercise in the heat (DE), stimulation of PV expansion with sodium citrate (CIT) supplementation would promote heart rate variability (HRV) recovery in endurance-trained men. Twelve participants lost 4% of body mass during DE. During subsequent 16-h recovery, participants consumed water ad libitum (CIT =5.5-L, PLC =5.1-L) and ate prescribed food supplemented with CIT or placebo in a randomized, double-blind, crossover manner. Relative changes in PV were assessed across DE and 16-h recovery. HRV was analyzed before and 16 h after DE in three conditions for altogether four 5-min periods: supine in a thermoneutral environment, supine in the heat (32°C, 46% relative humidity; 2 periods), and standing in the heat. A larger expansion of PV across 16-h recovery occurred in CIT compared to placebo trial (p < 0.0001). However, no between-trial differences appeared in HRV parameters (lnRMSSD, lnSDNN, lnLF/HF) in any 5-min period analyzed before or 16 h after DE (in all cases p > 0.05). Increases in HR (p < 0.001) and lnLF/HF (p = 0.005) and decreases in lnRMSSD (p < 0.001) and lnSDNN (p < 0.001) occurred following DE in both trials. Larger PV expansion induced by CIT supplementation after DE does not improve recovery of HRV at rest and has no influence on HRV responsiveness in endurance-trained men.

Using Predictive Modeling Technique to Assess Core Temperature Adaptations from Heart Rate, Sweat Rate, and Thermal Sensation in Heat Acclimatization and Heat Acclimation.

Assessing the adaptation of rectal temperature (Trec) is critical following heat acclimatization (HAz) and heat acclimation (HA) because it is associated with exercise performance and safety; however, more feasible and valid methods need to be identified. The purpose of this study was to predict adaptations in Trec from heart rate (HR), sweat rate (SR), and thermal sensation (TS) using predictive modeling techniques. Twenty-five male endurance athletes (age, 36 ± 12 y; VO2max, 57.5 ± 7.0 mL⋅kg-1⋅min-1) completed three trials consisting of 60 min running at 59.3 ± 1.7% vVO2max in a hot environment. During trials, the highest HR and TS, SR, and Trec at the end of trials were recorded. Following a baseline trial, participants performed HAz followed by a post-HAz trial and then completed five days HA, followed by a post-HA trial. A decision tree indicated cut-points of HR (<-13 bpm), SR (>0.3 L·h-1), and TS (≤-0.5) to predict lower Trec. When two or three variables met cut-points, the probability of accuracy of showing lower Trec was 95.7%. Greater adaptations in Trec were observed when two or three variables met cut-points (-0.71 ± 0.50 °C) compared to one (-0.13 ± 0.36 °C, p < 0.001) or zero (0.0 3 ± 0.38 °C, p < 0.001). Specificity was 0.96 when two or three variables met cut-points to predict lower Trec. These results suggest using heart rate, sweat rate, and thermal sensation adaptations to indicate that the adaptations in Trec is beneficial following heat adaptations, especially in field settings, as a practical and noninvasive method.

Corrigendum: Estrogen to Progesterone Ratio and Fluid Regulatory Responses to Varying Degrees and Methods of Dehydration.

[This corrects the article DOI: 10.3389/fspor.2021.722305.].

Estrogen to Progesterone Ratio and Fluid Regulatory Responses to Varying Degrees and Methods of Dehydration.

The purpose of this study was to investigate the relationship between volume regulatory biomarkers and the estrogen to progesterone ratio (E:P) prior to and following varying methods and degrees of dehydration. Ten women (20 ± 1 year, 56.98 ± 7.25 kg, 164 ± 6 cm, 39.59 ± 2.96 mL•kg•min-1) completed four intermittent exercise trials (1.5 h, 33.8 ± 1.3°C, 49.5 ± 4.3% relative humidity). Testing took place in two hydration conditions, dehydrated via 24-h fluid restriction (Dehy, USG > 1.020) and euhydrated (Euhy, USG ≤ 1.020), and in two phases of the menstrual cycle, the late follicular phase (days 10-13) and midluteal phase (days 18-22). Change in body mass (%BMΔ), serum copeptin concentration, and plasma osmolality (Posm) were assessed before and after both dehydration stimuli (24-h fluid restriction and exercise heat stress). Serum estrogen and progesterone were analyzed pre-exercise only. Estrogen concentration did not differ between phases or hydration conditions. Progesterone was significantly elevated in luteal compared to follicular in both hydration conditions (Dehy-follicular: 1.156 ± 0.31, luteal: 5.190 ± 1.56 ng•mL-1, P < 0.05; Euhy-follicular: 0.915 ± 0.18, luteal: 4.498 ± 1.38 ng·mL-1, P < 0.05). As expected, E:P was significantly greater in the follicular phase compared to luteal in both hydration conditions (Dehy-F:138.94 ± 89.59, L: 64.22 ± 84.55, P < 0.01; Euhy-F:158.13 ± 70.15, L: 50.98 ± 39.69, P < 0.01, [all •103]). Copeptin concentration was increased following 24-h fluid restriction and exercise heat stress (mean change: 18 ± 9.4, P < 0.01). We observed a possible relationship of lower E:P and higher copeptin concentration following 24-h fluid restriction (r = -0.35, P = 0.054). While these results did not reach the level of statistical significance, these data suggest that the differing E:P ratio may alter fluid volume regulation during low levels of dehydration but have no apparent impact after dehydrating exercise in the heat.

Cardiac autonomic modulation in type 1 diabetes during exercise-heat stress.

AIMS: Cardiac autonomic modulation, as assessed by heart rate variability (HRV), is independently attenuated by both type 1 diabetes (T1D) and exercise-heat stress, although their combined effects remain unclear. We therefore assessed HRV during exercise-heat stress in young individuals (18-37 years) with (n = 14) and without type 1 diabetes (n = 14). METHODS: Participants completed 30-min seated rest and three, 30-min bouts of semi-recumbent cycling at light, moderate, and vigorous metabolic heat productions (200, 250, 300 W/m2, respectively), each followed by 30-min recovery. Body core temperature (Tcore) and electrocardiogram were recorded throughout and analyzed during the final 5-min of rest and each exercise period. RESULTS: Relative to baseline, Tcore was increased in both groups, albeit to a greater extent in type 1 diabetes during vigorous exercise (T1D, 1.1 ± 0.3 °C; control, 0.8 ± 0.3 °C; P < 0.05). Overall HRV (as reflected by entropy) was attenuated throughout exercise relative to baseline in both groups, with the magnitude of the reduction greater in type 1 diabetes during vigorous exercise (T1D, - 108%; control, - 70%; P < 0.05). CONCLUSIONS: Given the negative correlations between decreased HRV and cardiac risk, our novel observations indicate that vigorous exercise in hot environments may pose a health concern for individuals with type 1 diabetes.

Application of evidence-based recommendations for heat acclimation: Individual and team sport perspectives.

Heat acclimation or acclimatization (HA) occurs with repeated exposure to heat inducing adaptations that enhance thermoregulatory mechanisms and heat tolerance leading to improved exercise performance in warm-to-hot conditions. HA is an essential heat safety and performance enhancement strategy in preparation for competitions in warm-to-hot conditions for both individual and team sports. Yet, some data indicate HA is an underutilized pre-competition intervention in athletes despite the well-known benefits; possibly due to a lack of practical information provided to athletes and coaches. Therefore, the aim of this review is to provide actionable evidence-based implementation strategies and protocols to induce and sustain HA. We propose the following suggestions to circumvent potential implementation barriers: 1) incorporate multiple induction methods during the initial acclimation period, 2) complete HA 1-3 weeks before competition in the heat to avoid training and logistical conflicts during the taper period, and 3) minimize adaptation decay through intermittent exercise-heat exposure or re-acclimating immediately prior to competition with 2-4 consecutive days of exercise-heat training. Use of these strategies may be desirable or necessary to optimize HA induction and retention around existing training or logistical requirements.

Effect of hypohydration on thermoregulatory responses in men with low and high body fat exercising in the heat.

It is unclear whether men with low body fat (LO-BF) have impaired thermoregulation during exercise heat stress compared with those with high body fat (HI-BF) when euhydration (EU) is maintained. Furthermore, in LO-BF individuals, hypohydration (HY) impairs thermoregulatory responses during exercise heat stress, but it is unknown whether this occurs in HI-BF counterparts. The purpose of this study was to test the hypotheses that men with HI-BF have impaired thermoregulatory responses to exercise heat stress and that HY further exacerbates these impairments vs. LO-BF. Men with LO-BF [n = 11, body mass (BM) 73.9 ± 8.5 kg, BF% 13.6 ± 3.8] and HI-BF (n = 9, BM 89.6 ± 6.9 kg, BF% 30.2 ± 4.1), in a randomized crossover design, performed 60 min of upright cycling in a hot environment (40.3 ± 0.4°C, relative humidity 32.5 ± 1.9%) at a metabolic heat production rate of 6 W/kg BM and finished exercise either euhydrated (EU; 0.3 ± 1.2 vs. 0.3 ± 0.9% BM loss) or HY (-2.5 ± 1.1 vs. -1.7 ± 1.5% BM loss). Changes in rectal temperature (ΔTrec), local sweat rate (ΔLSR), and cutaneous vascular conductance (ΔCVC; %max) were measured throughout. When EU, LO-BF and HI-BF had similar CVC and LSR responses (P > 0.05); however, LO-BF had a lower ΔTrec vs. HI-BF (0.92 ± 0.35 vs. 1.31 ± 0.32°C, P = 0.021). Compared with EU, HY increased end-exercise ΔTrec in LO-BF (0.47 ± 0.37°C, P < 0.01) but not in HI-BF (-0.06 ± 0.29°C, P > 0.05). HY, compared with EU, did not affect ΔLSR and ΔCVC in either group (P > 0.05). We conclude that, when euhydrated, men with HI-BF have a greater increase in Trec vs. LO-BF but similar CVC and LSR. HY exacerbates increases in Trec in LO-BF but not HI-BF. NEW & NOTEWORTHY: This is the first known investigation to compare thermoregulatory responses to exercise heat stress between men with high and low body fat (BF) in a physiologically uncompensable environment while simultaneously examining the confounding influence of hydration status. Both groups demonstrated similar sweating and cutaneous vasodilatory responses when euhydrated, despite vast differences in rectal temperature. Furthermore, in contrast to low BF, individuals with high BF demonstrated similar increases in core body temperature when either euhydrated or hypohydrated.

Downhill running and exercise in hot environments increase leukocyte Hsp72 (HSPA1A) and Hsp90α (HSPC1) gene transcripts.

Stressors within humans and other species activate Hsp72 and Hsp90α mRNA transcription, although it is unclear which environmental temperature or treadmill gradient induces the largest increase. To determine the optimal stressor for priming the Hsp system, physically active but not heat-acclimated participants (19.8 ± 1.9 and 20.9 ± 3.6 yr) exercised at lactate threshold in either temperate (20°C, 50% relative humidity; RH) or hot (30°C, 50% RH) environmental conditions. Within each condition, participants completed a flat running (temperate flat or hot flat) and a downhill running (temperate downhill or hot downhill) experimental trial in a randomized counterbalanced order separated by at least 7 days. Venous blood samples were taken immediately before (basal), immediately after exercise, and 3 and 24 h postexercise. RNA was extracted from leukocytes and RT-quantitative PCR conducted to determine Hsp72 and Hsp90α mRNA relative expression. Leukocyte Hsp72 mRNA was increased immediately after exercise following downhill running (1.9 ± 0.9-fold) compared with flat running (1.3 ± 0.4-fold; P = 0.001) and in hot (1.9 ± 0.6-fold) compared with temperate conditions (1.1 ± 0.5-fold; P = 0.003). Leukocyte Hsp90α mRNA increased immediately after exercise following downhill running (1.4 ± 0.8-fold) compared with flat running (0.9 ± 0.6-fold; P = 0.002) and in hot (1.6 ± 1.0-fold) compared with temperate conditions (0.9 ± 0.6-fold; P = 0.003). Downhill running and exercise in hot conditions induced the largest stimuli for leukocyte Hsp72 and Hsp90α mRNA increases.